Abstract
Aim High sensitive troponin (hs-TnI) levels may increase secondary to Coronavirus disease-2019 (COVID-19), and this increase is associated with cardiovascular mortality in COVID-19 patients. Epicardial adipose tissue (EAT) is associated with myocardial injury directly as a reservoir tissue for coronavirus, and indirectly through mediators it secretes as an apocrine gland. We aimed to evaluate the relationship between myocardial injury secondary to COVID-19 infection and EAT thickness.Material and methods Thoracic computed tomography (CT) was performed in 73 consecutive patients diagnosed with COVID-19. EAT thickness and volume were calculated by two radiologists blind to the study data. We formed two groups according to hs-TnI concentrations, patients with myocardial damage (hs-TnI ≥11.6 ng / l) and without myocardial damage (hs-TnI<11.6 ng / dl).Results A total of 46 patients were women (63.0 %). The mean age was 66.4±12.3 yrs in the myocardial injury group and 55.9±9.7 yrs in the group without myocardial injury (p<0.001). There were 20 hypertensive patients (68.9 %) in the injury group, while there were 12 hypertensive patients (27.3 %) in the group without injury (p=0.001). Glucose, C-reactive protein, D-dimer, white blood cell count, neutrophil, and neutrophil / lymphocyte ratio were higher in the injury group (p<0.05, for all variables). The mean EAT thickness was 5.6±1.6 mm in the injury group, whereas it was 4.8±1.8 mm in the group without injury (p=0.031). EAT thickness of 4.85 mm and above was associated with the myocardial injury with 65 % sensitivity and 39 % specificity (AUC=0.65, 95 % CI: 0.52-078, p=0.031).Conclusion In patients with COVID-19 infection, higher rates of myocardial injury were observed as the EAT thickness increased. Epicardial adipose tissue, contributes to cytokine-mediated myocardial injury either directly or indirectly by acting as a reservoir for coronavirus. Increased EAT thickness is associated with myocardial injury in COVID-19 patients.
Highlights
Coronavirus-2 (SARS-CoV-2) can affect the lungs by causing acute respiratory distress syndrome
Receiver Operating Characteristics (ROC) analysis demonstrated that Epicardial adipose tissue (EAT) thickness of 4.85 mm and above was associated with myocardial injury with 65 % sensitivity and 39 % specificity (AUC=0.65, 95 % CI: 0.52–0.078, p=0.031; Figure 3)
The imbalance between anti and proinflammatory adipokines released from EAT may play a role in the formation of a cytokine storm [25]. These findings show that EAT plays a key role in the myocardial injury that may develop in COVID-19 patients due to angiotensin-converting enzyme 2 (ACE2) and a cytokine storm
Summary
Coronavirus-2 (SARS-CoV-2) can affect the lungs by causing acute respiratory distress syndrome. Coronavirus disease-2019 (COVID-19) can cause multiple organ involvement, including the cardiovascular system [1, 2]. COVID-19 has caused significant morbidity and mortality. As the COVID-19 pandemic threatens global health, learning about the pathogenesis and clinical course of the disease can help to set therapeutic goals and to define the clinical approach. Inflammation is a crucial factor in the development and progression of COVID-19 [3]. Studies have shown that inflammatory parameters, such as C-reactive protein (CRP), effectively predict the clinical severity of COVID-19 [4, 5]. Identifying parameters that provide information about inflammation status is essential for understanding the clinical course and prognosis of COVID-19
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